Immune cell-specific and common molecular signatures in rheumatoid arthritis through molecular network approaches

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dc.authoridComertpay, Betul/0000-0002-3515-1461
dc.authoridGOV, ESRA/0000-0002-5256-4778
dc.contributor.authorComertpay, Betul
dc.contributor.authorGov, Esra
dc.date.accessioned2025-01-06T17:44:11Z
dc.date.available2025-01-06T17:44:11Z
dc.date.issued2023
dc.description.abstractRheumatoid arthritis (RA) is an autoimmune disorder and common symptom of RA is chronic synovial inflammation. The pathogenesis of RA is not fully understood. Therefore, we aimed to identify underlying common and distinct molecular signatures and pathways among ten types of tissue and cells obtained from patients with RA. In this study, transcriptomic data including synovial tissues, macrophages, blood, T cells, CD4+T cells, CD8+T cells, natural killer T (NKT), cells natural killer (NK) cells, neutrophils, and monocyte cells were analyzed with an integrative and comparative network biology perspective. Each dataset yielded a list of differentially expressed genes as well as a reconstruction of the tissue-specific protein-protein interaction (PPI) network. Molecular signatures were identified by a statistical test using the hypergeometric probability density function by employing the interactions of transcriptional regulators and PPI. Reporter metabolites of each dataset were determined by using genome-scale metabolic networks. It was defined as the common hub proteins, novel molecular signatures, and metabolites in two or more tissue types while immune cell-specific molecular signatures were identified, too. Importantly, miR-155-5p is found as a common miRNA in all tissues. Moreover, NCOA3, PRKDC and miR-3160 might be novel molecular signatures for RA. Our results establish a novel approach for identifying immune cell-specific molecular signatures of RA and provide insights into the role of common tissue-specific genes, miRNAs, TFs, receptors, and reporter metabolites. Experimental research should be used to validate the corresponding genes, miRNAs, and metabolites.
dc.description.sponsorshipAdana Alparslan Turkes Science and Technology University Scientific Research Projects Committee (BAPKO) [19103010]; YOK 100/2000 Doctoral Fellowship Program
dc.description.sponsorshipThis research was supported by grants from Adana Alparslan Turkes Science and Technology University Scientific Research Projects Committee (BAPKO) in the context of project 19103010. The scholarships under the YOK 100/2000 Doctoral Fellowship Program provided to BC are greatly acknowledged.
dc.identifier.doi10.1016/j.biosystems.2023.105063
dc.identifier.issn0303-2647
dc.identifier.issn1872-8324
dc.identifier.pmid37852410
dc.identifier.scopus2-s2.0-85174254677
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.biosystems.2023.105063
dc.identifier.urihttps://hdl.handle.net/20.500.14669/2966
dc.identifier.volume234
dc.identifier.wosWOS:001094418100001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Sci Ltd
dc.relation.ispartofBiosystems
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241211
dc.subjectRheumatoid arthritis
dc.subjectTranscriptome
dc.subjectImmune cell-specific signatures
dc.subjectNetwork biology
dc.titleImmune cell-specific and common molecular signatures in rheumatoid arthritis through molecular network approaches
dc.typeArticle

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